Infection and HLA-G Molecules in Nasal Polyposis
Sinonasal polyposis (SNP) is a chronic inflammatory pathology with an unclear aetiopathogenesis. Human papillomavirus (HPV) infection is one candidate for the development of SNP for its epithelial cell trophism, hyperproliferative effect, and the induction of immune-modulatory molecules as HLA-G. We...
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2014-01-01
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Series: | Journal of Immunology Research |
Online Access: | http://dx.doi.org/10.1155/2014/407430 |
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author | Roberta Rizzo Nicola Malagutti Daria Bortolotti Valentina Gentili Antonella Rotola Enrico Fainardi Teresa Pezzolo Claudia Aimoni Stefano Pelucchi Dario Di Luca Antonio Pastore |
author_facet | Roberta Rizzo Nicola Malagutti Daria Bortolotti Valentina Gentili Antonella Rotola Enrico Fainardi Teresa Pezzolo Claudia Aimoni Stefano Pelucchi Dario Di Luca Antonio Pastore |
author_sort | Roberta Rizzo |
collection | DOAJ |
description | Sinonasal polyposis (SNP) is a chronic inflammatory pathology with an unclear aetiopathogenesis. Human papillomavirus (HPV) infection is one candidate for the development of SNP for its epithelial cell trophism, hyperproliferative effect, and the induction of immune-modulatory molecules as HLA-G. We enrolled 10 patients with SNP without concomitant allergic diseases (SNP-WoAD), 10 patients with SNP and suffering from allergic diseases (SNP-WAD), and 10 control subjects who underwent rhinoplasty. We analyzed the presence of high- and low-risk HPV DNA and the expression of membrane HLA-G (mHLA-G) and IL-10 receptor (IL-10R) and of soluble HLA-G (sHLA-G) and IL-10 by polyp epithelial cells. The results showed the presence of HPV-11 in 50% of SNP-WoAD patients (OR:5.5), all characterized by a relapsing disease. HPV-11 infection was absent in nonrelapsing SNP-WoAD patients, in SNP-WAD patients and in controls, supporting the hypothesis that HPV-11 increases risk of relapsing disease. HPV-11 positive SNP-WoAD patients presented with mHLA-G and IL-10R on epithelial cells from nasal polyps and showed secretion of sHLA-G and IL-10 in culture supernatants. No HLA-G expression was observed in HPV negative polyps. These data highlight new aspects of polyposis aetiopathogenesis and suggest HPV-11 and HLA-G/IL-10 presence as prognostic markers in the follow-up of SNP-WoAD. |
format | Article |
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institution | Kabale University |
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language | English |
publishDate | 2014-01-01 |
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series | Journal of Immunology Research |
spelling | doaj-art-2d7fd99848b84160a8f378beca2834ef2025-02-03T07:25:43ZengWileyJournal of Immunology Research2314-88612314-71562014-01-01201410.1155/2014/407430407430Infection and HLA-G Molecules in Nasal PolyposisRoberta Rizzo0Nicola Malagutti1Daria Bortolotti2Valentina Gentili3Antonella Rotola4Enrico Fainardi5Teresa Pezzolo6Claudia Aimoni7Stefano Pelucchi8Dario Di Luca9Antonio Pastore10Section of Microbiology and Medical Genetics, Department of Medical Sciences, University of Ferrara, Via Luigi Borsari, 46, 44121 Ferrara, ItalyOperative Unit of Otolaryngology, St. Anna Hospital, Via A. Moro, 844124 Ferrara, ItalySection of Microbiology and Medical Genetics, Department of Medical Sciences, University of Ferrara, Via Luigi Borsari, 46, 44121 Ferrara, ItalySection of Microbiology and Medical Genetics, Department of Medical Sciences, University of Ferrara, Via Luigi Borsari, 46, 44121 Ferrara, ItalyOperative Unit of Otolaryngology, St. Anna Hospital, Via A. Moro, 844124 Ferrara, ItalyOperative Unit of Neuroradiology, St. Anna Hospital, Via A. Moro, 844124 Ferrara, ItalyOperative Unit of Otolaryngology, St. Anna Hospital, Via A. Moro, 844124 Ferrara, ItalyOperative Unit of Otolaryngology, St. Anna Hospital, Via A. Moro, 844124 Ferrara, ItalyOperative Unit of Otolaryngology, St. Anna Hospital, Via A. Moro, 844124 Ferrara, ItalySection of Microbiology and Medical Genetics, Department of Medical Sciences, University of Ferrara, Via Luigi Borsari, 46, 44121 Ferrara, ItalyOperative Unit of Otolaryngology, St. Anna Hospital, Via A. Moro, 844124 Ferrara, ItalySinonasal polyposis (SNP) is a chronic inflammatory pathology with an unclear aetiopathogenesis. Human papillomavirus (HPV) infection is one candidate for the development of SNP for its epithelial cell trophism, hyperproliferative effect, and the induction of immune-modulatory molecules as HLA-G. We enrolled 10 patients with SNP without concomitant allergic diseases (SNP-WoAD), 10 patients with SNP and suffering from allergic diseases (SNP-WAD), and 10 control subjects who underwent rhinoplasty. We analyzed the presence of high- and low-risk HPV DNA and the expression of membrane HLA-G (mHLA-G) and IL-10 receptor (IL-10R) and of soluble HLA-G (sHLA-G) and IL-10 by polyp epithelial cells. The results showed the presence of HPV-11 in 50% of SNP-WoAD patients (OR:5.5), all characterized by a relapsing disease. HPV-11 infection was absent in nonrelapsing SNP-WoAD patients, in SNP-WAD patients and in controls, supporting the hypothesis that HPV-11 increases risk of relapsing disease. HPV-11 positive SNP-WoAD patients presented with mHLA-G and IL-10R on epithelial cells from nasal polyps and showed secretion of sHLA-G and IL-10 in culture supernatants. No HLA-G expression was observed in HPV negative polyps. These data highlight new aspects of polyposis aetiopathogenesis and suggest HPV-11 and HLA-G/IL-10 presence as prognostic markers in the follow-up of SNP-WoAD.http://dx.doi.org/10.1155/2014/407430 |
spellingShingle | Roberta Rizzo Nicola Malagutti Daria Bortolotti Valentina Gentili Antonella Rotola Enrico Fainardi Teresa Pezzolo Claudia Aimoni Stefano Pelucchi Dario Di Luca Antonio Pastore Infection and HLA-G Molecules in Nasal Polyposis Journal of Immunology Research |
title | Infection and HLA-G Molecules in Nasal Polyposis |
title_full | Infection and HLA-G Molecules in Nasal Polyposis |
title_fullStr | Infection and HLA-G Molecules in Nasal Polyposis |
title_full_unstemmed | Infection and HLA-G Molecules in Nasal Polyposis |
title_short | Infection and HLA-G Molecules in Nasal Polyposis |
title_sort | infection and hla g molecules in nasal polyposis |
url | http://dx.doi.org/10.1155/2014/407430 |
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